3. Contents:
▪ Introduction
▪ Periodontal disease
▪ Epidemiology
- Distribution of periodontal disease
- Factors responsible for periodontal disease
- Determinants of periodontal disease
- Host
- Agent
- Environment
▪ Conclusion
▪ References
3
World
India
4. Introduction
4
▪ The periodontium, defined as those tissues supporting and
investing the tooth, comprises of cementum, periodontal
ligament, bone lining the tooth socket (alveolar bone), and
that part of the gingiva facing the tooth (dentogingival
junction).
8. Epidemiology
Epidemiology is the study of distribution and determinants of
health related states or events in specified populations, and
application of this study to control health problems.
Epidemiologic studies are conducted to
Describe the health status of populations
Elucidate the etiology of diseases
Identify risk factors
Forecast disease occurrence
Assist in disease prevention and control
8
10. 10
The Periodontal Disease Classification System of the
American Academy of Periodontology (AAP), 1999
NormanO. Harris ,Primary Preventive Dentistry, Pearson publishers, 2017; 8th edition: Pg 69-86.
11. Classification of periodontal diseases
and conditions
11Gary C. Armitage Development of a Classification System for Periodontal Diseases and Conditions, Ann Periodontol, 1999; 4(1).
12. Classification of periodontal diseases
and conditions
12Gary C. Armitage Development of a Classification System for Periodontal Diseases and Conditions, Ann Periodontol, 1999; 4(1).
14. Gingival diseases Periodontal diseases
Plaque induced gingival diseases Chronic periodontitis
Non- plaque – induced gingival lesions Agressive periodontitis
Periodontitis as a manifestation of
systemic disease
14
Soben Peter. Essentials of Preventive andCommunity Dentistry, 5th ed. New Delhi : Arya Publishing House, 2013
15. Uses of epidemiology in study of
periodontal diseases
To study historically rise and fall of disease
To diagnose community problems of health and disease by study and
analysis of incidence, prevalence and morbidity
To estimate individuals risk and chances of developing disease
To help complete the clinical picture and natural history of disease by
group analysis
To identify clinical syndromes by observation of group behavior
15
16. To evaluate need and effectiveness of health services
To search for causes of disease and of health by observation of group
habits, customs and models of life.
Work upon it has been retarded by a number of factors.
Greatest incidence late in life
16
17. ▪ Difficulty in objective measurement.
- Gingivitis – subjective error
- Pocket depth - observational errors
- Alveolar bone loss - cannot be evaluated clinically
17
19. Gingivitis
▪ At population level, found in early childhood, is more
prevalent and severe in adolescence.
▪ Ubiquitious in children and adults
- 82% US adolescents – overt gingivitis and signs of gingival
bleeding
- 75% of adults – gingival bleeding, dental calculus and poor
oral hygiene
▪ Similar in other parts of world
19
20. Chronic periodontitis
(Non aggressive form of Periodontitis)
▪ Most prevalent among adults and seniors
▪ Children and adolescents – wide range of frequency in
various geographic regions and racial / ethnic groups
▪ Relatively high frequency in Africa and Latin America
▪ Low disease frequency – young Caucasians in Western
Europe and North America
20
21. ▪ 11-25 years age group
Prevalence
1-3%Western Europe
2-5 % North America
4-8% South America
5-8%Asia
10-20% Africa
Racial/ ethnic
1-3% Caucasians
5-8% Asians
5-10% Hispanics and Latin Americans
8-20% Africans and African Americans
21
22. North America
United States of America
▪ Health Examination Survey (1960-62)
- 18-79 yr
- 48.5 % - gingivitis
- 25.4 % - periodontal pockets
- 1.13 – PI per person
▪ NHANES –I (1971-74)
- 6-74 yr
- 25% - gingivitis ; 4.5% - 1-3 mm pocket ; 12.1% - >4mm
- 0.83 – PI per person
22
23. ▪ NIDR (1985-86)
- 18-64 yr
- 44% - > 1 site bleeding ; 13.4 % - >1 site pockets 4-6mm;
43.8 % - AL >3 mm
▪ NHANES – III (1988-94)
- 13 & older
- 54 % BOP ; 21 % - pockets > 4mm ; 38.1 % AL > 3mm.
23
24. Canada
▪ Broduer JM et al (2001)
- Quebec, 35-44 yr ; 2110
- 45.6 % - > 4mm pocket ; 8.5% - > 6mm pocket
- 81 % gingival bleeding
▪ Locker et al (1998)
- Ontario, 13-15 yr ; 721
- Dental calculus – 44.6 % Canadian born ;
- 72.9 % immigrants.
24
25. Europe
▪ Higher % of adults have moderate probing depth and
mild-moderate periodontal attachment loss
13-54% of 35-44 year old - 3.5 -5.5 mm pocket
Sheiham A et al 2002
▪ > 3.5 mm attachment loss
42% 35-44 year old
70% 55-64 year old
Morris AJ et al 2001
25
26. ▪ Increase prevalence of periodontal disease is seen in in
Eastern Europe as compared to Western Europe
▪ 35-44 yr
- Shallow pockets
- East Europe – 45%
- West Europe – 36 %
- Deep pockets
- East Europe – 30 %
- West Europe – 10 %
26
27. Central And South America
▪ Credible data scarce
38%-67% - moderate or advanced periodontitis
28-52% Moderate disease
4-19% Severe disease
Gjermo P et al 2002
▪ Southern Brazil 30 years and older
> 5 mm attachment loss 79%
> 7 mm attachment loss 52%
▪ Poor oral hygiene
▪ Periodontitis widespread among older age groups- 70-100%
- > 50 years - moderate and chronic periodontitis
Susin S et al 2004
27
28. Africa
▪ Poor oral hygiene
▪ Abundant calculus
▪ High prevalence of moderate probing depth and
attachment loss
▪ 30 years and older
> 4 mm attachment loss
44%-84% Uganda
79-98% Tanzania
91-99% Kenya
BaelumV et al 2002
28
29. Asia and Oceania
▪ 80-100% - calculus
▪ Low and lower middle income countries
shallow probing depth deep pockets
< 25 years 0-20% < 2%
> 60years 67% 20-30%
▪ Increase prevalence of gingival bleeding, dental calculus,
low prevalence of healthy periodontal status irrespective
of age cohort or country level of development
29
30. Early-onset aggressive
periodontitis
▪ Age group 11-25 year
Prevalence
Western Europe 0.1-0.5%
North America 0.4-0.8%
South America 0.3-1%
Asia 0.4-1%
Africa 0.5-5%
Racial/ ethnic
Caucasians 0.1-0.2%
Asians 0.4-1%
Hispanics and Latin Americans 0.5-1%
Africans and African Americans 1-3%
30
31. Gingival recession
▪ USA
> 3mm recession – 35% 30-90 year old
75% 65-90 year old
> 5 mm recession 23% 65-90 year old
31
33. Among School Children
33
Author
name
Year Study
population
Sample
size
Age
group
Results
Marshall-Day
&Tandon
1940 middle class
children, Lahore
756 ≥13 68. 6 % - gingivitis
Marshall-Day
& Shourie
1944 low & middle class 613 5-15 80 % - gingivitis
Shick 1960 Low middle class 807 5-19 74.59 % gingivitis
Greene 1960 low
socioeconomic
1613 11-17 96.3 % gingivitis, 1.3 %
with bone resorption.
Ramfjord 1960 Bombay 827 11- 17 100 % - gingivitis
Urban – PDI – 1.42
Rural – PDI – 2.41
Dutta A 1965 Calcutta 1424 6-12 Gingivitis- 73.4 % in 6
yr, 96.5 % in 12 yr.
Tewari et al 1979 Chandigarh 1511 6-16 92.46 % - periodontal
disease
34. Among School Children
34
Author
name
Year Study
population
Sample
size
Age
group
Results
Nagaraj Rao
et al
1980 Udupi 500 28 % - marginal gingivitis,
7.2 % - chronic generalized
gingivitis.
Srivastava
RP
1989 Jhansi 690 6-18yrs 6-8 yr – 42% ;
15-17 yr – 94.02%
Rao SP et al 1993 2 U, 2 R and 2
T primary
schools-
Wardha
60.8 % Manjan
Pdl disease higher in tribal
Goel P et al 2000 Puttur
municipality
200 in
each
group
5-6 yrs,
12-13yrs
- 5-6 years old – no calculus
- 47.78% - 12-13 years –
calculus
Christensen
LB et al
2003 Bhopal 599 - 11-13
yrs
15 % healthy gingiva
91% rural children
CPI score 2(Calculus)
35. Adult Population
35
Author
name
Year Study
population
Sample
size
Age
group
Results
Marshall Day
& Shourie
1940 Punjab and
north India
60 % chronic peridontitis
Mehta et al 1953 Bombay &
Ratnagiri
2219 males 18-55 Severity - with age and in
Low SES
Greene 1960 1613 males
India, 577
males
Atlanta
18-30 -63% males – rural India,
-highly prevalent in both
groups.
-Indian Rural – more severe
periodontal disease.
Gupta et al 1962 Trivandrum 800 11-50 100 % > 30 yr.
90 % - 11-30 yr.
Ramachandr
an et al
1973 Tamil Nadu 6647rural,
1536-urban
Rural-95.3%
Uraban-95.5%
36. Adult Population
36
Author
name
Year Study
population
Sample
size
Age
group
Results
Shetty &
Gururaja Rao
1987 urban & rural
areas – South
Canara
2510 17-60 31.3 % -periodontitis ; 67.13% -
Chronic gingivitis, rural more
than urban.
Anil S et al 1990 Trivandrum 15-44 15-19 yr – 86% - calculus &
bleeding
25-29 yr – 80% - shallow
pocketing
35-44 yr – 33% - pockets >
6mm.
Kurian M et
al
1996 Hebri 1513 15 yr 0.4 % - healthy periodontium
1.6 % - Bleeding on probing
26.6 % - Shallow pockets
24.1 % - deep pockets
JagdeesanM
et al
2000 Women, Rural,
Pondicherry
1100 > 15
years
< 30 years – 15.8%
> 30 years – 73.9%
37. Adult Population
37
Author
name
Year Study
population
Sample
size
Age
group
Results
DoifodeV
et al
2000 Field practice
area,Bapunagar,
Nagpur
- 5061
residents
34.8% - periodontal disease
Srikanth G
et al
2000 fishermen
community,
Malpe, Udupi
300 ≥ 15 91% - periodontal disease
Rao A 1999 Institutionalize,>
60 years,
Mangalore
300 Calculus – 21.88%; shallow
pockets – 32.29%
Deep pockets – 15.1%
Shah N,
Sundaram
KR
2004 South Delhi 1240 > 60 CPITN
Bleeding on probing-7.4%
Calculus - 1.7%
Shallow pockets - 19%
Deep pockets - 71.9%
38. Handicapped Children
38
Author
name
Year Study
population
Sample
size
Age
group
Results
Mehrotra
AK et al
1982 61-physically
handicapped,
66- mentally
retarded
physically handicapped -
88.5 %
mentally retarded
individuals -100%
Tandon S
& Sudha P
1986 40 handicapped
children
8-18 showed poorer oral
hygiene as compared to
normal.
Vyas &
Damle
1991 466 11-14 100% - mentally
subnormal
95.95 % - juvenile
delinquents
97.38 % - physically
handicapped
Bhavsar JP
and Damle
SG
1995 Bombay 593 12-14 Bleeding and calculus
component are high
39. Pregnant women
39
Author
name
Year Study
population
Sample
size
Age
group
Results
Samanth
Asha
1976 40 – in each
trimester
40 non-
pregnant,
Chandigarh
80 -Mean gingivitis-
Pregnant women
-maximum change – 2nd
trimester
Dixit J et al 1980 80 pregnant 40
non-pregnant
women
120 severity of gingivitis in
pregnant subjects.
Sequeira
PS
1991 170 pregnant
women
170 -7.6 %
- No significant differences
in different trimesters
42. ▪ In India, data from the National Oral Health Survey (2002-
2003) states that in children aged 12 years, the prevalence
of periodontal disease was 57% and in the 15 year age
group, it was 67.7%. the prevalence was 89.6% and 79.9%
in the 35-44 yrs and 65-74yrs.
42
43. Percent of subjects with
Periodontal disease in India
by age
57%
67.70%
89.60%
79.90%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
12 yrs 15 yrs 35-44 yrs 65-74 yrs
43
44. Mean no. of sextants with
periodontal disease by age in India
2
2.9
4.5
2.9
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
5
12 years 15 years 35-44 years 65-74 years
44
45. Percent of subjects with loss of
attachment by age in India
0%
10%
20%
30%
40%
50%
60%
70%
15 yrs 35-44 yrs 65-74 yrs
7%
41.20%
60.70%
45
46. Mean no. of Sextants with loss of
attachment by age in India
0.2
1.3
1.6
0
0.2
0.4
0.6
0.8
1
1.2
1.4
1.6
1.8
15 years 35-44 years 65-74 years
46
49. Host Agent Environment
•Age
•Sex
•Race/Ethnicity
•Genetics
•Intra-oral variations
•Endocrine changes
•Local host factors
•Occupational habits
and neuroses
•Concomitant
disease
•Emotional
disturbance
•Bacteria
•Plaque
•Calculus
•Chemical and
physical hazards
•Geographic areas
•Nutrition
•Fluoride
•Degree of
urbanization
•Education
•Socio economic
status
•Cultural factors
•Professional dental
care
Epidemiological triad
49
50. Host Factors
▪ The prevalence of periodontal diseases indirectly and steadily increases
with age.
▪ Chronic destructive periodontal disease is associated wth older groups.
▪ There is a steady progression in alveloar boneloss with increasing age.
▪ Gingivitis worsens with boneloss as boneloss is conducive to gingivitis
because of abnormal contour it produces
▪ But it is difficult to measure because of age changes and also gingivitis is
reversible depending on oral hygiene status and plaque accumulation
50
AGE
51. ▪ In general females have less periodontal disease than males though the
difference is not great.
▪ But relatively high incidence of juvenile periodontitis has been found in
females.
▪ Gingivitis is also prevalent in boys than girls however during puberty it is
more commonly seen in girls
▪ In some under developed countries periodontal disease is worse in
females than males due to frequent child birth, ill health, poor nutrition
and poor oral hygiene measures.
51
Gender
52. ▪ Many Indian studies (Dutta A et al, Nanda RS et al,
Dolwani R et al, Pathak S et al) – Periodontal disease is
more in males comapred to females.
▪ Shah N et al, DoifodeV et al – no gender differences
▪ DCI 2002-2003- no gender differences
52
53. ▪ Some studies have shown greater prevalance and severity of
periodontal disease among blacks than whites.
Russell et al – greater prevalence and severity of pdl disease is
seen among blacks than white
NIDR (National institute of development and research) Survey-
whites blacks
18-24yrs 15 % 17 %
55-64yrs 76 % 90 %
53
Race
54. - In patients with actalasia, hypophosphataemia or cyclic
neutropenia, the prevalence of periodontal disease is
more.
- Study of 169 twin pairs concluded that about half of the
variance in periodontitis was attributable to heredity.
54
Genetic
55. Bossert & Marks
- Upper molars & lower central incisors – frequently
affected teeth followed by lower molars.
- Lower bicuspids & upper canines – least affected.
Loe & associates
- interproximal areas – more severely affected – upper arch
- Lingual area – lower arch
Tewari et al 1979 – lower anterior teeth
55
Intraoral variations
56. - An increase in gingivitis among children noted as they
approach puberty (Massler, Russell)
- Females - pregnancy & menstruation
- Periodontitis is aggravated in endocrinal imbalances like
Hyperparathyroidism, hyperparathyroidism
Diabetes- Nearly one third of diabetics are found to have
severe periodontal disease.
▪ In fact periodontal disease is known as 6th complication of
diabetes (Loe 1993) 56
Endocrinal changes
57. ▪ Dental calculus
formation
▪ Dental caries lesion
near gingival tissue
▪ Oral hygiene pattern
▪ Alveolar bone
morphology
▪ Gingival form
57
▪ Traumatic occlusion
- Food impaction
- Disuse
▪ Tooth morphology and
alignment
▪ Form and location of
tooth furcation
▪ Level and quality of
dental restorations
▪ Contact between teeth
and other local
anatomic factors
Local Host factors
58. ▪ Oral Hygiene Practices
-Causal relationship between poor oral hygiene and
gingivitis (Loe & co workers)
-with periodontitis less – gingivitis not always –
periodontitis
▪ Oral hygiene pattern
Pathak S et al 2000 – brushing twice daily had lower
gingivitis and periodontitis
58
59. Occupational habits like holding nails in the mouth among
carpenters and upholsteres, thread biting among tailors
Oral habits like bruxism, fingernail biting, pencil biting, mouth
breathing etc
Faulty tooth brushing results in cervical abrasion, gingival
trama and gingival recession and leads to gingivitis finally
progressing to periodontitis.
59
Habits
60. Tobacco
Smoking
▪ 2- 7 fold increase in risk in smokers (Bergstrom et al 1994, Grossi SC et
al 1997,Tomar SL et al 2000)
▪ Cigarette smoking along with poor oral hygeine increases the risk of
periodontal disease.
▪ Nicotine in cigarette has an affect on the circulatory system by
decreasing blood supply and intake of oxygen by heamoglobin thus
reducing the body’s ability to fight infection and increases alveolar
bone resorption.
▪ DoifodeV et al 2000- 5061 residents, Nagpur
periodontal disease
Smokers 47.8%
Non – smokers 34.2%
60
61. Smokeless tobacco
- gingival recession and white mucosal lesions
▪ DoifodeV et al 2000
Periodontal disease
Tobacco chewers 44.4%
Non – tobacco chewers 32.4%
Gutkha 46.1%
Non – gutkha 33.3%
Betel leaf 37.9%
Non betel leaf chewers 33.1%
61
62. - Diabetes & heavy metal poisoning
-Leukemia & anemia
- HIV infections
-Debilitating diseases
62
Concomitant disease
63. ▪ Diabetes
-Type I andType II
- risk factor – exaggerated host response
- metabolic control
Type II – Pima Indians – Gila river community in Arizona- 2-3 times higher
risk of developing destructive periodontal disease (Emrich et al 1991)
- Chavada MG et al 1993
60 non – diabetic, 62 non controlled diabetes male 30-66 years
OHI PI
Cases 3.8 4.9
Controls 3.5 4.2
63
64. Mechanism
Vascular changes
Polymorphonuclear leukocyte dysfunction
Abnormal collagen synthesis
Cytokine production
Genetic
Impaired salivary flow
▪ HIV infection
- necrotizing ulcerative periodontitis
- related to immunosuppression status
- pathogenic bacteria
64
65. ▪ Osteoporosis
Krejci CB et al 2002
CAL – greater in osteoporotic women.
▪ Cardiovascular diseases
-chronic inflammation anywhere-affect heart.
-periodontal pathogens – directly injure vascular
endothelium - favor platelet aggregation and
thromboembolic events
-c-reactive protein is a risk factor for cardiovascular disease-
high levels in periodontitis.
65
66. Pneumonia and COPD
▪ Oral colonization by respiratory pathogens, fostered by
poor oral hygiene and periodontal diseases, appears to be
associated with nosocomial pneumonia.
▪ The results associating periodontal disease and COPD are
preliminary and large-scale longitudinal and epidemiologic
RCTs are needed. Scannapieco FA et al 2003
66
67. Related with necrotizing Periodontal diseases
Mehrotra AK et al (1982)
- 61-physically handicapped - 88.5 %
- 66- mentally retarded individuals -100%
Genco et al 1999 psychological stress, distress and coping behavior
financial strain OR 1.7 attachment loss / alveolar bone loss
inadequate coping OR 2.2 attachment loss
OR 1.9 alveolar bone loss
Significant risk indicator
-Psychosocial measures of stress associated with financial strain and
distress
67
Psychological/ Emotional disturbance / challenged
patients
68. Dental Plaque- also called as a host associated biofilm, is a sticky yellowish
white deposit containing numerous bacteria, mucus, food particles and
other irritants found on the surface of teeth.
68
Agent Factors
69. Calculus- It acts as a predisposing factor in the aetiology of periodontal
diseases by virtue of the presence of dental plaque in its surface rather
than playing an active and direct role on itself in aetiology of
periodontitis.
Bacterial flora- Actinomycetes actinomyces, Porphyromonas gingivalis,
Human CMV and other herpes viruses
Chemical and physical hazards- mercury, lead, thallium – dark line
parallel to gingival margin , alveolar resorption
- Radium and other sources of ionizing radiation – alveolar damage
and loosening of teeth
- Medication- dilantin sodium
69
70. Russell
- High – Chile, Lebanon, JordanThailand, Burma,
Malaya, Ceylon, India &Trinidad
- Intermediate – US (Blacks), Ecuador, Colombia, Ethiopia.
- Low – US (White)
70
Environmental Factors
Geographic areas
71. 70% of adults - degree of gingivitis and periodontitis
Data collected 1980 onwards – WHO global oral data bank
▪ Gingivitis and calculus deposits – more prevalent and
severe in low income nations;
▪ Fewer global difference in prevalence of severe
peiodontitis
71
72. Physical nature
- Coarse & fibrous food – beneficial (Mehta et al, Borle et al)
- Lower prevalence in non-vegetarians (Thaha et al,1986)
Deficiencies of Vit A, B complex, C & D & Ca & P
-Vit C – gingival bleeding – not known – bone loss or CAL
- No evidence to support use of nutrients in treatment of
periodontitis.
72
Diet and nutrition
73. Russell – severity less in fluoridated areas
Anuradha KP et al 2002
283 36 -45 year old
mean plaque
Shammur 0.5 ppm F 1.45
kendawada 1.1 ppm F 1.21 p< 0.001
Halebathi 3.1 ppm F 1.12
No effect on calculus
Decrease in shallow and deep pockets with increase in F
73
Fluoride
74. - Slightly higher in rural areas than in urban areas
- DCI – 2002 – 2003
- More prevalent in lower socioeconomic group
- Historically - lower SES
- Gingivitis & poor oral hygiene and subgingival calculus
related to lower SES (Mehta et al, Zaveri et al)
- Lack of awareness, inaccessibility to dental services,
inability to afford costly treatments, inadequate diet
74
Degree of Urbanization
Socio economic status
75. - Inversely related to increasing levels of education
- This may be due to more systematic home care and dental
maintenance care found among the educated people
75
Education
77. ▪ Periodontal surveys enable the determination of the
prevalence, extent and severity of the periodontal diseases in
populations and can generally be conducted in reasonable
time frame at relatively moderate cost.
▪ A better understanding of the causal relationship between
risk factors and occurrence of disease, epidemiologic studies
form the basis of the disciplines of risk assessment and
disease control.
▪ Clear picture of the disease, its determinants and time trends
yield vital data which will be greatly helpful to assess the
current scenario and planning for the future preventive
programmes at a population level.
77
78. Risk Factors for periodontal
diseases
▪ “Risk" is defined as "the probability that some harmful event
will occur"
▪ The term risk factor is defined as
An attribute or exposure that is significantly associated with
the development of a disease
A determinant that can be modified by intervention, thereby
reducing the possibility of occurence of disease or other
specified outcomes.
▪ Risk predictors/ markers, although associated with increased
risk for disease, do not cause the disease.
78
79. ▪ Risk marker/Predictors: an attribute or exposure that is
associated with increased probability of disease, but is not
necessarily a causal factor.
▪ Risk Determinant: an attribute or exposure that increases the
probability of occurrence of disease or other specified
outcome.
▪ Modifiable risk factor: a determinant that can be modified by
intervention, thereby reducing the probability of disease
79
Brian A. Burt. Definitions of Risk. Journal of Dental Education. 2001; Vol 65 (10): 1007-8
80. 80
Causative factors
• Smoking
• Alcohol
• Poor oral
hygiene
practices
Predictive factors
(Statistical sense)
• illiteracy
• Socioeconomic
status
• Race
Modifiable factors
• Habits like
smoking,
alcohol, oral
hygeine
practices, nail
biting
• Serum levels of
Vitamin D
• Harmonal levels
in puberty and
pregnancy
• Drugs like
phenytoin
Unmodifiable
factors
• Age
• sex
• race
• genetic factors
• hereditary
diseases.
K. Park,Text book of preventive and social medicine -23rd edition, Jabalpur: Banarsidas Bhanot
2015 pg no: 38.
According to K. Park risk factors for periodontal disease are
divided as:
81. Risk Factors Risk
Determinants/
Background
Characteristis
Risk Indicators Risk Markers/
Predictors
Tobacco smoking Genetic factors HIV/AIDS Previous history
of periodontal
disease
Diabetes Age and Gender Osteoporosis Bleeding on
probing
Pathogenic
bacteria
Stress Infrequent dental
visit
Microbial tooth
deposits
Socioeconomic
status
81
Newman, Carranza’s Clinical Periodontology, Elsevier publishers, 11th edition, 2012, pg.no.472-474.
Risk Elements for Periodontal
Disease
82. Clinical Risk Assessment for
Periodontal Disease
Demographic Data Medical History Dental History Clinical Examination
Age
•Duration of exposure to risk
elements
•Postmenopausal women
•Evidence of agrresive
periodontitis
Diabetes Family history of early
tooth loss
•Genetic predisposition to
aggressive disease
Plaque accumulation
•Microbial sampling for
putative periodontal
pathogens
Gender
•Preventive practices
•Frequency of care
Tobacco smoking Previous history of
periodontal disease
Calculus
SES
•Dental awareness
•Frequency of care
HIV/AIDS Frequency of dental
care
Tooth examination
Osteoporosis Bleeding on probing
Stress Extent of loss of
attachment loss
•Aggressive forms of disease
Tooth examination
•Plaque retentive areas
• Anatomic factors
Restorative factors
82
Newman, Carranza’s Clinical Periodontology, Elsevier publishers, 11th edition, 2012, pg.no.472-474.
83. Reviews
▪ A significant association between Vitamin D deficiency and periodontal status
was found in only current smokers. Smoking could modify the effect of vitamin D
on periodontitis. Vitamin D serum levels may be a risk indicator of susceptibility to
periodontitis because it could be related to bone mineral density through its
regulation of calcium homeostasis and attribute to anti-inflammatory effects
Hyo-Jin Lee (2015)
▪ A high prevalence of periodontitis in US adults aged 30 years and older.
Prevalence was greater in Non-Hispanic Asians than Non-Hispanic whites,
although lower than other minorities as Non Hispanics Asians are greatly
associated with increased poverty level and education. Hence race is also a risk
factor for the incidence of periodontal disease. Paul I. Eke (2015)
83
84. ▪ Environmental tobacco smoke (ETS) is a mixture of mainstream
(smoke exhaled by the smoker) and sidestream (smoke given off
by a burning cigarette) smoke, and both have similar chemical
constituents. Exposure to ETS has increased chance of association
with periodontal disease.
Aderonke A. Akinkugb (2016)
▪ Systemic review with metaanalysis (Heiko Zimmermann 2015) - A
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A relatively low plaque control record (PCR) could be correlated to
an effective oral hygiene due to daily habit of tooth brushing.
84
85. ▪ Area of residence emerged as a strong socioeconomic predictor of prevalence of
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slums were less pronounced . Manu Raj Mathur (2017)
▪ Age, Gender and socioeconomic status were strongly associated with clustering.
People in the older age group had a greater clustering of risk indicators, this could
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covered teeth by competing for calcium ions, known to be important in
the bridging between acidic groups on the pellicle surface and the
bacterial cell walls.
▪ Fluoride decreases the dissolution rate of enamel during acid attack,
preserves the apatitic structure, and facilitates remineralization of tooth
structure.
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95.
96. Mean number of sites with gingival
bleeding
betel chewers smokers nontobacco users
22.6+/-21.8 10.8+/11.2 8.7+/-6.8
p<0.0001
▪ Gingival bleeding - Betel chewers (55.1%) smokers (27.6%).
▪ Betel chewing and gingival bleeding +(OR=2.41)
▪ Smoking and gingival bleeding -(OR=0.75)
▪ Oral hygiene had the strongest relationship with gingival bleeding
(OR=18.11).
Amarasena N et al 2003
96